Subclinical Coronary Atherosclerosis Research Articles

The Clinical Value of High-Intensity Signals on the Coronary Atherosclerotic Plaques: Noncontrast T1-Weighted Magnetic Resonance Imaging

Over the past several decades, significant progress has been made in the pathohistological assessment of vulnerable plaques and in invasive intravascular imaging techniques. However, the assessment of plaque morphology by invasive modalities is of limited value for the detection of subclinical coronary atherosclerosis and the subsequent prediction or prevention of acute cardiovascular events. Recently, magnetic resonance (MR) imaging technology has reached a sufficient level of spatial resolution, which allowed the plaque visualization of large and static arteries such as the carotids and aorta. However, coronary wall imaging by MR is still challenging due to the small size of coronary arteries, cardiac and respiratory motion, and the low contrast-to-noise ratio between the coronary artery wall and the surrounding structures. Following the introduction of carotid plaque imaging with noncontrast T1-weighted imaging (T1WI), some investigators have reported that coronary artery high-intensity signals on T1WI are associated with vulnerable plaque morphology and an increased risk of future cardiac events. Although there are several limitations and issues that need to be resolved, this novel MR technique for coronary plaque imaging could influence treatment strategies for atherothrombotic disease and may be useful for understanding the pathophysiological mechanisms of atherothrombotic plaque formation.

Obstructive sleep apnea is independently associated with subclinical coronary atherosclerosis among middle-aged women.

Obstructive sleep apnea (OSA) is associated with coronary disease among men. However, this association is not clear for women. In this study, we evaluate the association between OSA and presence of subclinical atherosclerosis assessed by tomographic coronary calcium score in middle-aged women. We evaluated consecutive women aged between 45 and 65years in perimenopause or postmenopause period (with menstrual irregularity-amenorrhea > 60days), without manifest cardiovascular disease (heart failure, coronary disease, and stroke), from two gynecologic clinics. All patients underwent clinical evaluation, computed tomographic examination for coronary artery calcium (CAC > 100 Agatston units), and portable sleep study. Multiple logistic regression models were used to evaluate the association between OSA and CAC, controlling for traditional risk factors including Framingham Risk Score (FRS), body mass index (BMI), and diabetes. We studied 214 women (age 56years (52-61); BMI 28kg/m2 (25-31), 25% diabetes, 62% hypertension). OSA (apnea-hypopnea index (AHI) ≥5 events/h) was diagnosed in 82 women (38.3%). CAC was more prevalent in patients with moderate/severe OSA (AHI ≥15 events/h) than in patients without or with mild OSA, 19% vs 4.5 and 1.6%, respectively (p < 0.01). Moderate to severe OSA was associated with CAC in unadjusted (odds ratio = 6.25, 95% CI 1.66-23.52; p < 0.01) and adjusted (odds ratio = 8.19, 95% CI 1.66-40.32; p = 0.01) logistic regression analysis. Moderate to severe OSA is independently associated with the presence of CAC in middle-aged women. These results reinforce the concept that women are also susceptible to the cardiovascular consequences of OSA.

The effects of multiple coronary artery disease risk factors on subclinical atherosclerosis in a rural population in the United States

IntroductionThe risk factors for cardiovascular disease (CVD) are associated with coronary atherosclerosis and having multiple risk factors potentiates atherosclerosis. This study examined the prevalence of multiple biological and lifestyle/behavioral risk factors and their association with coronary artery calcium (CAC), a marker for subclinical coronary atherosclerosis. MethodsThis is a cross-sectional study of 1607 community-dwelling asymptomatic individuals from central Appalachia who participated in CAC screening between January 2011 and December 2012. Data on demographics (sex and age) and 7 traditional risk factors for coronary artery disease (CAD) were collected and categorized into 5 groups (0–1, 2, 3, 4, and ≥5). Prevalence of these risk factors and CAC scores (0, 1–99, 100–399, ≥400) were assessed, and the impact of the number of risk factors on CAC scores were delineated using multiple logistic regression. ResultsOver 98% of participants had ≥1 risk factor. While obesity, diabetes, hypertension, and family history of CAD significantly increased the odds of having CAC, CAC scores significantly increased with number of risk factors. After adjusting for demographic factors, having 3, 4, and ≥5 risk factors was significantly associated with increased odds of having higher CAC scores when compared to zero CAC score by more than one and half times [OR=1.65, CI (1.20–2.25)], two times [OR=2.32, CI (1.67–3.23)] and three times [OR=3.45, CI (2.42–4.92)], respectively. ConclusionThe high prevalence of multiple risk factors in the study population suggests the need for aggressive multiple risk factors interventions for primary prevention of CAD, which could address CVD health disparities.

PD47-08 CORONARY ARTERY CALCIUM SCORE AND ASSOCIATION WITH RECURRENT NEPHROLITHIASIS: THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS

You have accessJournal of UrologyStone Disease: Epidemiology & Evaluation II1 Apr 2016PD47-08 CORONARY ARTERY CALCIUM SCORE AND ASSOCIATION WITH RECURRENT NEPHROLITHIASIS: THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS Ryan Hsi, Andrew Spieker, Marshall Stoller, David Jacobs, Alex Reiner, Robyn McClelland, Arnold Kahn, Thomas Chi, Moyses Mzklo, and Mathew Sorensen Ryan HsiRyan Hsi More articles by this author , Andrew SpiekerAndrew Spieker More articles by this author , Marshall StollerMarshall Stoller More articles by this author , David JacobsDavid Jacobs More articles by this author , Alex ReinerAlex Reiner More articles by this author , Robyn McClellandRobyn McClelland More articles by this author , Arnold KahnArnold Kahn More articles by this author , Thomas ChiThomas Chi More articles by this author , Moyses MzkloMoyses Mzklo More articles by this author , and Mathew SorensenMathew Sorensen More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.2696AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Kidney stone disease is linked to systemic conditions including hypertension, obesity, diabetes mellitus, and coronary heart disease. Therefore, biologic pathways that result in coronary artery calcification may also lead to the development of nephrolithiasis. Subclinical coronary artery calcification (CAC) is an established predictor of cardiovascular events. CAC is quantified noninvasively by computed tomography, and the calculated CAC score reflects the presence and extent of atherosclerotic disease. While a history of kidney stones has been linked to subclinical carotid atherosclerosis, no study has examined its relationship with CAC. We studied the association between kidney stone history and prevalent CAC from the MESA study. METHODS The Multi-Ethnic Study of Atherosclerosis is a multi-site cohort study of participants aged 45-84 without known cardiovascular disease at baseline (2000-2002). At follow up in 2010-2012, 3,282 participants underwent computed tomography to determine CAC and had kidney stone history assessed by self-report. CAC scores were categorized as none, mild (<100), moderate (101-400), or severe (>400). A cross-sectional analysis was performed adjusting for demographic and dietary factors related to kidney stones. RESULTS Prevalence of kidney stone disease history was approximately 9%, mean age was 69.5±9.3 years, 39% of participants were Caucasian, 47% were men, and 69% had detectable (CAC score >0). Of the stone formers, 129 (44.6%) reported a history of 2 or more stones in the past. Mean±SD CAC score among non-stone formers and stone formers was 279±595 and 380±602, respectively. No difference in CAC score was seen between single stone formers and non-stone formers. Recurrent kidney stone formation was associated with moderate or severe CAC on multivariable logistic regression (versus none or mild CAC) (OR 1.80, 95% CI 1.22-2.67). When CAC scores were separated into none, mild, moderate, and severe CAC, recurrent stone formation was associated with higher CAC score category on multivariable ordinal logistic regression (OR per category 1.44, 95% CI 1.04- 2.01). CONCLUSIONS Recurrent kidney stone formation is associated with subclinical coronary atherosclerosis. This association appeared stronger with CAC severity than with CAC presence. The clinical significance of these findings is that a recurrent stone former, who has no prior cardiac history and is otherwise asymptomatic, may have higher levels of coronary calcification and be at risk for future cardiovascular events. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e1173 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Ryan Hsi More articles by this author Andrew Spieker More articles by this author Marshall Stoller More articles by this author David Jacobs More articles by this author Alex Reiner More articles by this author Robyn McClelland More articles by this author Arnold Kahn More articles by this author Thomas Chi More articles by this author Moyses Mzklo More articles by this author Mathew Sorensen More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

HIV Infection Itself May Not Be Associated With Subclinical Coronary Artery Disease Among African Americans Without Cardiovascular Symptoms.

BackgroundThe key objectives of this study were to examine whether HIV infection itself is associated with subclinical coronary atherosclerosis and the potential contributions of cocaine use and antiretroviral therapies (ARTs) to subclinical coronary artery disease (CAD) in HIV‐infected persons.Methods and ResultsBetween June 2004 and February 2015, 1429 African American (AA) adults with/without HIV infection in Baltimore, Maryland, were enrolled in an observational study of the effects of HIV infection, exposure to ART, and cocaine use on subclinical CAD. The prevalence of subclinical coronary atherosclerosis was 30.0% in HIV‐uninfected and 33.7% in HIV‐infected (P=0.17). Stratified analyses revealed that compared to HIV‐uninfected, HIV‐infected ART naïve were at significantly lower risk for subclinical coronary atherosclerosis, whereas HIV‐infected long‐term ART users (≥36 months) were at significantly higher risk. Thus, an overall nonsignificant association between subclinical coronary atherosclerosis and HIV was found. Furthermore, compared to those who were ART naïve, long‐term ART users (≥36 months) were at significantly higher risk for subclinical coronary atherosclerosis in chronic cocaine users, but not in those who never used cocaine. Cocaine use was independently associated with subclinical coronary atherosclerosis.ConclusionsOverall, HIV infection, per se, was not associated with subclinical coronary atherosclerosis in this population. Cocaine use was prevalent in both HIV‐infected and ‐uninfected individuals and itself was associated with subclinical disease. In addition, cocaine significantly elevated the risk for ART‐associated subclinical coronary atherosclerosis. Treating cocaine addiction must be a high priority for managing HIV disease and preventing HIV/ART‐associated subclinical and clinical CAD in individuals with HIV infection.

Serum oxidized low-density lipoprotein decreases in response to statin therapy and relates independently to reductions in coronary plaque in patients with HIV

Circulating oxidized low-density lipoprotein (oxLDL) levels are elevated in HIV-infected patients and have been associated with atherosclerosis. Statins have been shown to reduce plaque on coronary computed tomography angiography (cCTA) in HIV-infected individuals. Thus, we investigated the effect of statins on serum oxLDL levels and the relationship between changes in oxLDL and coronary atherosclerosis on cCTA in patients with HIV. We previously conducted a 12-month randomized, placebo-controlled trial with atorvastatin in 40 HIV-infected patients on stable antiretroviral therapy with subclinical coronary atherosclerosis and low-density lipoprotein (LDL)-cholesterol less than 130 mg/dl. In the current analysis, patients underwent cCTA and measurements of serum oxLDL, sCD14, sCD163, lipoprotein phospholipase-A2, and fasting lipids at baseline and end of the study. Nineteen patients were randomized to atorvastatin and 21 patients to placebo. Serum oxLDL decreased -22.7% (95% CI -28.7 to -16.7) in the atorvastatin group and increased 7.5% (95% CI -3.3 to 18.4) in the placebo group (P < 0.0001). Change in oxLDL significantly correlated with changes in noncalcified plaque volume, total plaque volume, positively remodeled plaque, and low attenuation plaque. The association between changes in oxLDL and noncalcified plaque volume was independent of the baseline 10-year Framingham risk, LDL, CD4 cell count, and viral load. Statins lower oxLDL levels in HIV-infected patients, and reductions in oxLDL are related to improvements in coronary atherosclerosis, independent of traditional cardiovascular risk factors. Reductions in oxLDL may be one mechanism through which statins exert beneficial effects on reducing atherosclerosis in HIV-infected individuals.

Initiation of PCSK9 inhibition in patients with heterozygous familial hypercholesterolaemia entering adulthood: a new design for living with a high-risk condition?

According to current estimates, as many as 4.5 million people in Europe suffer from the heterozygous form of familial hypercholesterolemia (HeFH).1 Their plasma concentration of low-density lipoprotein cholesterol (LDL-C) is two to three times above normal from birth, and accordingly, if untreated, the risk of coronary heart disease (CHD) and acute myocardial infarction (AMI) is markedly increased compared with non-HeFH populations.1 Indeed, in the pre-statin era, a clinical study on the incidence of CHD in patients with molecularly defined HeFH showed that the mean age of onset of symptomatic CHD was 42 ± 7 (SD) years for men and 48 ± 11 years for women, and that the corresponding ages at the time of first AMI were 47 ± 12 and 59 ± 13 years, respectively ( Figure 1 ).2 The early onset of clinically significant CHD in the pre-statin era is understandable, since the plasma concentration of LDL-C strongly elevated from birth. It also explains the early onset of subclinical coronary atherosclerosis in these patients. Thus, extrapolation of coronary angiographic data from HeFH males and HeFH females predicted that, on average, coronary stenosis starts at 17 and 25 years of age, respectively ( Figure 2 ).3 Corresponding non-invasive data have been obtained recently by assessing accumulation of coronary plaque burden with computed tomography angiography in a HeFH patient population on suboptimal statin therapy, which had been initiated in adulthood.4 When the plaque burden was extrapolated to age, the data suggested that atherosclerotic plaques may start to develop in HeFH males and females at a mean age of ∼20 and 30 years, respectively. Moreover, the total plaque burden significantly predicted future coronary …

Decreased Renal Function Is a Risk Factor for Subclinical Coronary Atherosclerosis in Korean Postmenopausal Women.

ObjectivesDecreased renal function is associated with increased cardiovascular risk. Our study was planned to verify the association of decreased renal function and subclinical coronary atherosclerosis in postmenopausal women.MethodsWe performed a retrospective review of 251 Korean postmenopausal women who visited the health promotion center for a routine health checkup. Estimated glomerular filtration rate (eGFR) was used to show renal function, which was estimated by calculated using the Cockcroft-Gault (CG) and the modification of diet in renal disease (MDRD) formulas. Coronary atherosclerosis was assessed by 64-row multidetector computed tomography.ResultsWomen with reduced eGFR (< 60 mL/minute/1.73 m2) had significantly higher brachial-ankle pulse wave velocity (baPWV) than women with normal eGFR (≥ 60 mL/minute/1.73 m2). The eGFR was negatively correlated with baPWV (r = -0.352, P < 0.001), significantly. The eGFR was lower in women with coronary atherosclerosis than in normal control women, markedly. Reduced eGFR was significantly associated with the presence of coronary atherosclerosis (odds ratio [OR] = 7.528, 95% confidence interval [CI] = 2.728-20.772, P < 0.001).ConclusionsDecreased eGFR was closely associated with increased arterial stiffness and coronary atherosclerosis in postmenopausal women. Evaluating subclinical atherosclerosis by screening the renal function in postmenopausal women may be helpful screening high risk group and considering starting menopausal hormone therapy before atherosclerosis development.

Association of Homocysteine Levels with Subclinical Coronary Atherosclerosis in Asymptomatic Subjects

This article is available from http://www.labmedonline.org 2016, Laboratory Medicine Online This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Progression of atherosclerotic plaques is known to be correlated with elevated circulating homocysteine (Hcy). However, whether the level of Hcy is related with coronary atherosclerosis in the subclinical state is unclear. Therefore, we performed this study to investigate the relationship between blood Hcy levels and subclinical atherosclerosis in asymptomatic self-referred subjects. Methods: We retrospectively enrolled 2,968 self-referred asymptomatic subjects (1,374 men, 1,594 women) who had undergone both coronary CT angiography (CCTA) and coronary artery calcium scoring. The relationships between atherosclerosis, Hcy, and other clinical factors were assessed. Results: Higher levels of Hcy were related with age, male gender, body mass index (BMI), waist circumference, blood pressure, high density lipoprotein (HDL), triglyceride, blood glucose, HbA1c, hsCRP, and coronary artery calcium score (CACS). Coronary plaque was more frequently found in higher Hcy quartile groups (21.3%, 28.8%, 34.4%, and 34.3%, P 50%) was also more frequent in higher Hcy quartile groups (1.8%, 5.4%, 5.0%, and 6.6%, P 400) than the first quartile group. Conclusions: Blood Hcy levels were associated with an increased risk of the presence and extent of subclinical atherosclerosis in asymptomatic subjects.

Brazilian adult individuals with untreated isolated GH deficiency do not have accelerated subclinical atherosclerosis.

GH and its principal mediator IGF1 have important effects on metabolic and cardiovascular (CV) status. While acquired GH deficiency (GHD) is often associated with increased CV risk, the consequences of congenital GHD are not known. We have described a large group of patients with isolated GHD (IGHD) due to a homozygous mutation (c.57+1G>A) in the GH releasing hormone receptor gene, and shown that adult GH-naïve individuals have no evidence of clinically evident premature atherosclerosis. To test whether subclinical atherosclerosis is anticipated in untreated IGHD, we performed a cross-sectional study of 25 IGHD and 27 adult controls matched for age and gender. A comprehensive clinical and biochemical panel and coronary artery calcium scores were evaluated by multi-detector tomography. Height, weight, IGF1, homeostasis model assessment of insulin resistance, creatinine and creatininekinase were lower in the IGHD group. Median and interquartile range of calcium scores distribution was similar in the two groups: IGHD 0(0) and control 0(4.9). The vast majority of the calcium scores (20 of 25 IGHD (80%) and 18 of 27 controls (66.6%)) were equal to zero (difference not significant). There was no difference in the calcium scores classification. None of IGHD subjects had minimal calcification, which were present in four controls. Three IGHD and four controls had mild calcification. There were two IGHD individuals with moderate calcification and one control with severe calcification. Our study provides evidence that subjects with congenital isolated lifetime and untreated severe IGHD do not have accelerated subclinical coronary atherosclerosis.

Association of Elevations of Specific T Cell and Monocyte Subpopulations in Rheumatoid Arthritis With Subclinical Coronary Artery Atherosclerosis.

Coronary artery disease (CAD) is the leading cause of excess deaths in rheumatoid arthritis (RA). However, identification of features denoting patients with a risk of developing CAD is lacking. The composition of circulating peripheral blood mononuclear cell (PBMC) subsets in RA patients differs markedly from that in healthy controls with regard to the extent of T cell activation, with clonal expansion and differentiation to effector memory status, and presence of inflammatory monocytes. In this study, we sought to evaluate whether elevations in these PBMC subpopulations in RA patients could denote those with an increased risk of subclinical CAD, as determined by the presence of coronary artery calcification (CAC). The study cohort comprised 72 patients with RA who underwent cardiac computed tomography to assess CAC. PBMC subsets were determined by multiparameter flow cytometry. Multivariable logistic regression was used to determine the associations between PBMC subpopulations and the presence of CAC. Among the 72 patients with RA, 33% had CAC and exhibited significant increases in the levels of circulating CD4 T cell subsets denoting activation and differentiation to the effector memory phenotypes. Analogous increases in the levels of CD8 T cell subsets, as well as in the CD14(high)CD16+ intermediate monocyte subset, were also present in these patients, as compared to those without CAC. The increases in the CD4 and CD8 T cell subsets were highly intercorrelated, whereas the increases in CD14(high)CD16+ monocytes were independent of elevations in the CD4 T cell subsets. After adjustments for relevant confounders, the levels of CD4+CD56+CD57+ T cells and CD14(high)CD16+ monocytes remained associated with the presence of CAC. These findings indicate that PBMC subsets are markers for the presence of CAC and suggest that mechanisms of atherogenesis in RA may operate in part through the elevations in these subsets, raising further questions about the mechanisms underlying the presence of such alterations in cell composition in patients with RA and the potential for shared etiologic pathways between RA and cardiovascular disease.

Osteoprotegerin, but Not Receptor Activator for Nuclear Factor-κB Ligand, is Associated With Subclinical Coronary Atherosclerosis in HIV-Infected Men.

Abnormalities in the osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) axis have been observed in HIV-infected persons and have been implicated in cardiovascular disease (CVD) pathogenesis in the general population. To determine associations of serum OPG and RANKL concentrations with HIV infection and subclinical atherosclerosis. Cross-sectional study nested within the Multicenter AIDS Cohort Study. Four US academic medical centers. There were 578 HIV-infected and 344 HIV-uninfected men. Coronary artery calcium (CAC) was measured by noncontrast cardiac computed tomography, and coronary stenosis and plaque characteristics (composition, presence, and extent) were measured by coronary computed tomography angiography. All statistical models were adjusted for traditional CVD risk factors. OPG concentrations were higher, and RANKL concentrations were lower among HIV-infected men compared with HIV-uninfected men (P < 0.0001 each). Among HIV-infected men, higher OPG concentrations were associated with the presence of CAC, mixed plaque, and coronary stenosis >50%, but not with plaque extent. In contrast, among HIV-uninfected men, higher OPG concentrations were associated with the extent of both CAC and calcified plaque, but not with their presence. RANKL concentrations were not associated with plaque presence or the extent among HIV-infected men, but among HIV-uninfected men, lower RANKL concentrations were associated with greater extent of CAC and total plaque. OPG and RANKL are dysregulated in HIV-infected men, and their relationship to the presence and extent of subclinical atherosclerosis varies by HIV status. The role of these biomarkers in CVD pathogenesis and risk prediction may be different in HIV-infected men.

RISK ASSESSMENT MODEL FOR CORONARY ATHEROSCLEROSIS IN PATIENTS WITH VISCERAL OBESITY

Aim. To invent a model for coronary atherosclerosis risk prediction in patients with visceral obesity and to conduct comparison research for this model with the other known Framingham and PROCAM. Material and methods. Totally 67 men included, of the age 40-65 (50,95±6,54 y.o.) without angina pectoris and clinical signs of another localization atherosclerosis. Patients had general obesity of I-III grade with BMI 35,16±3,32 kg/m , and visceral obesity by the thickness of epicaridal fat >7 mm. After coronary arteriography or multidetector computed tomography of coronary arteries we selected 2 comparison groups: group I (n=25) — patients with coronary atherosclerosis, group II (n=42) — without. For the invention of the prognostic score we used regression model with regression and optimal scaling. Results. Potential predictors of coronary atherosclerosis riskas a result of two groups comparison were: arterial hypertension, carbohydrate metabolism disorders, triglycerides, leptin, adiponectin and C-rective protein. As the result of regression analysis each predictor got its own significance mark. The rate of correctclassifications reached 79,1% that shows good prognostic value of this regression model. While using Framingham and PROCAM model the prognostic value of subclinical coronary atherosclerosis was 24,6% and 21,6% lower, resp., than the new risk assessment. Conclusion. The model invented of the risk assessment in visceral obesity patients makes it possible to take into account the main pathogenetic mechanisms that connect obesity and coronary atherosclerosis.

Arterial Stiffness Index and Coronary Artery Plaques in Patients with Subclinical Coronary Atherosclerosis.

Arterial stiffness is a physiologic quantitative value used to measure arterial compliance. It is predictive of coronary atherosclerosis in patients with intermediate to high cardiovascular risk. However, a correlation between arterial stiffness and subclinical coronary atherosclerosis has yet to be established. Therefore, the purpose of this study was to evaluate arterial stiffness using an arterial stiffness index (ASI) and investigate its association with coronary artery plaque in patients with subclinical coronary atherosclerosis. Our study enrolled 156 consecutive subjects who underwent health screening using a 64-slice cardiac computed tomography angiography (CCTA). Their arterial stiffness index was assessed noninvasively by CardioVision(®) MS-2000. The atheroma on the coronary vessel walls was analyzed. Of the 156 patients, 53 displayed at least one > 50% stenotic lesion over the coronary arteries in CCTA images. The patients with at least one > 50% coronary stenotic plaque were older and had higher systolic blood pressure and ASI values than patients without > 50% coronary stenotic plaque. After dividing the study population into 2 groups by those patients over and under 50 years of age, the ASI positively correlated with the presentation of at least one > 50% coronary stenotic plaque in patients aged ≥ 50 years (odds ratio = 1.02, 95% confidence interval: 1.00-1.04, p = 0.03). The ASI could play a role in risk stratification systems for coronary artery disease in patients with subclinical coronary atherosclerosis, and is a useful clinical marker for the correlation of early coronary plaque. Arterial stiffness; Arterial stiffness index; Atherosclerosis; Coronary artery plaque.

Abstract 11134: Subclinical Coronary Plaque Burden in Asymptomatic Relatives of Patients With Documented Premature Coronary Artery Disease

Introduction: A family history of premature coronary artery disease (CAD) is a well-known risk factor for adverse coronary events with age of onset being inversely related to the degree of heritability. Hypothesis: We hypothesized that asymptomatic first degree relatives, of patients with premature CAD, suffer a high burden of subclinical coronary atherosclerosis. Methods: First degree relatives, aged 30-65 years, of patients with a documented coronary revascularization procedure before the age of 40 years, were invited to participate in the study. Participants were matched by age, sex and absence of a family history, with patients referred for coronary CT angiography (CTA) because of atypical angina or non-anginal chest pain. A pooled blinded analysis was performed. The main outcome measure was the number of plaque-affected coronary segments. Results: 88 relatives and 88 symptomatic controls underwent CTA. Treatment of hypertension and dyslipidemia tended to be more common among controls (p=0.06). 4 relatives reported vague symptoms of which none had angiographic signs of obstructive CAD (any luminal stenosis above 50%). The calculated SCORE risk among relatives was generally low (85% having a 10-year risk of ≤1%). Relatives had significantly (p=0.006) more affected segments than controls (0 segments: 29,6% vs. 48,9%, 1-2 segments: 27,3% vs. 31,8%, 3-5 segments: 23,9% vs. 11,4% and ≥6 segments: 19,3% vs. 8,0%). In a multivariable logistic regression analysis, the presence of any CAD (OR 3.16 (1.50;6.70)) as well as non-calcified plaques (OR 2.2 (1.14;4.26)), mixed plaques (OR 6.77 (2.7;16.98)) and calcified plaques (OR 2.34 (1.01;5.43)) were more frequent. Although increased, the presence of obstructive plaques, however, did not differ statistically significantly between relatives and controls (OR 2.58 (0.85;7.83)). Conclusions: Asymptomatic relatives of patients with premature CAD suffer a high coronary plaque burden even when compared with symptomatic patients with an a priori higher risk of CAD. Our results indicate a strong genetic component in the genesis of coronary atherosclerosis and, moreover, underline the limitations of current guidelines on prevention of CAD.

Family history of diabetes and the risk of subclinical atherosclerosis

AimThis study investigated the influence of a family history of diabetes on the risk of subclinical coronary atherosclerosis according to coronary computed tomography angiography (CCTA) in asymptomatic individuals. MethodsA total of 6434 consecutive asymptomatic individuals with no prior history of coronary artery disease voluntarily underwent CCTA evaluation as part of a general health examination. Coronary atherosclerotic plaque and significant coronary artery stenosis (degree of stenosis ≥50%) on CCTA were assessed. Logistic regression analysis was used to determine the association between a family history of diabetes and atherosclerotic plaque or significant coronary artery stenosis according to the degree of diabetes (normal, prediabetic and diabetic). ResultsMean age of study participants was 53.7±7.6 years, and 4694 (73.0%) were male. A total of 1593 (24.8%) participants had a family history of diabetes in a first-degree relative. Among the study participants, 1115 (17.3%), 3122 (48.5%) and 2197 (34.1%) were categorized as diabetic, prediabetic and normal, respectively. In diabetic participants, after stepwise adjustments for clinical and laboratory variables, a family history of diabetes was significantly associated with non-calcified plaque (P<0.05 for all), but did not appear to be associated with either calcified or mixed plaques or with significant coronary artery stenosis (P>0.05 for all). In prediabetic and normal participants, a family history of diabetes was not associated with either atherosclerotic plaque or significant coronary artery stenosis (P>0.05 for all). ConclusionIn asymptomatic diabetic individuals, a family history of diabetes is consistently associated with non-calcified coronary plaque after adjusting for risk factors.

Coronary Artery Calcium Score and Association with Recurrent Nephrolithiasis: The Multi-Ethnic Study of Atherosclerosis

Subclinical coronary artery calcification is an established predictor of cardiovascular events. While a history of kidney stones has been linked to subclinical carotid atherosclerosis, to our knowledge no study has examined its relationship with coronary artery calcification. We studied the association between kidney stone history and prevalent coronary artery calcification in MESA (Multi-Ethnic Study of Atherosclerosis). MESA is a multisite cohort study of participants 45 to 84 years old without known cardiovascular disease at baseline from 2000 to 2002. Computerized tomography was done in 3,282 participants at followup in 2010 to2012 to determine coronary artery calcification and kidney stone history was assessed by self-report. Coronary artery calcification scores were categorized as none-0, mild-1 to 99, moderate-100 to 399 or severe-400 or greater. Cross-sectional analysis was performed adjusting for demographic and dietary factors related to kidney stones. The prevalence of kidney stone disease history was approximately 9%, mean ± SD participant age was 69.5 ± 9.3 years, 39% of participants were Caucasian, 47% were men and 69% had detectable coronary artery calcification (score greater than 0). No difference in the score was seen between single stone formers and nonstone formers. Recurrent kidney stone formation was associated with moderate or severe calcification on multivariable logistic regression vs none or mild calcification (OR 1.80, 95% CI 1.22-2.67). When coronary artery calcification scores were separated into none, mild, moderate and severe calcification, recurrent stone formation was associated with a higher score category on multivariable ordinal logistic regression (OR 1.44 per category, 95% CI 1.04-2.01). Recurrent kidney stone formation is associated with subclinical coronary atherosclerosis. This association appeared stronger with coronary artery calcification severity than with coronary artery calcification presence.

Traumatic brain injury, coronary atherosclerosis and cardiovascular mortality

Background: Traumatic-brain-injury (TBI) is a devastating-condition resulting in cerebral edema and ischemia. This study investigates the association of mild-TBI (mTBI) to sub-clinical atherosclerosis and cardiovascular (CV) mortality.Methods: Five hundred and forty-three veterans without known coronary artery disease or diagnosed mental disorder, who underwent coronary artery calcium (CAC) scanning for clinical indications, were followed for a median of 4-years. Veterans' medical diagnoses and neuropsychiatric health status (mTBI vs non-mTBI) were evaluated using VA electronic medical records. CAC was defined as 0, 1–100, 101–400 and 400+.Results: CAC was higher in mTBI, compared to without-mTBI (p < 0.05). TBI was more prevalent with the-severity of CAC (p < 0.05). Regression-analyses revealed that mTBI is an independent-predictor of CAC (p < 0.01). The CV mortality rate was 25% in mTBI and 10.5% in without-mTBI (p = 0.0001). Multivariable survival regression analyses revealed a significant-association between mTBI and CAC, with increased-risk of CV mortality (p < 0.05). The hazard-ratio of CV mortality was 5.25 in mTBI & CAC > 0, compared to without-mTBI & CAC = 0 (p < 0.05). The risk of CV-mortality was 2.25 for mTBI & CAC = 1–100, 4.93 for mTBI & CAC = 101–400 and 7.06 for mTBI & CAC ≥ 400, compared to matched CAC-categories without-mTBI (p < 0.05). The area under ROC curve to predict CV mortality was 0.64 for mTBI, 0.69 for mTBI & PTSD, 0.85 for mTBI & CAC > 0 and 0.92 for the combination. The prognostication of mTBI to predict CV mortality is superior to the Framingham risk score. Also the combination of mTBI & PTSD provided incremental prognostic values to predict CV mortality (p < 0.05).Conclusions: mTBI is associated with the severity of sub-clinical coronary atherosclerosis and independently predicts CV mortality.

Visceral adipose tissue influences on coronary artery calcification at young and middle-age groups using computed tomography angiography.

Purpose:The purpose of the study was to evaluate the impact of excessive visceral adipose tissue (VAT) on subclinical coronary atherosclerosis and coronary artery calcifications (CAC) in young and middle-age groups using multislice computed tomography.Methods:This study is a single center, cross-sectional study. Eligible patients (n = 159), who under the age of 61 years, with chest pain and mild to moderate probability to have coronary artery disease (CAD) were enrolled. Coronary calcium score and epicardial adipose tissue (EAT) were measured at the level of the left main coronary artery while VAT was measured at the level of the iliac crest.Results:The average age was (48 ± 8 years). The mean VAT was (38 ± 21 cm2) with no significant difference between men and women (38 ± 22 vs. 37 ± 19 P = 0.8) respectively. Student's t-test analysis showed significantly higher VAT in patients with detectable CAC than patients with no CAC (48 ± 24 vs. 33 ± 18 P = 0.00002), respectively. Univariate regression analysis showed that VAT and EAT, are strong predictor for CAC (hazard ratio [HR] 1.034, 95% confidence interval [CI: 1.016–1.052]. P <0.001 and [HR] 1.344, 95% CI: [1.129–1.601] P = 0.001), respectively.Conclusion:Excessive VAT is significantly associated with positive CAC. VAT can strongly predict subclinical CAD in individuals at young and middle-age groups.

Assessment risks of subclinical coronary atherosclerosis at patients with obesity

Assessment risks of subclinical coronary atherosclerosis at patients with obesity